Pacemakers are perhaps the most well known devices that provide chronic electrical stimulus, such as cardiac rhythm management. Modern pacemakers are designed to be implanted within a patient receiving the medical therapy. Other examples of cardiac stimulators include implantable cardiac defibrillators (ICDs) and implantable devices capable of performing pacing and defibrillating functions. Such implantable devices provide electrical stimulation to selected portions of the heart in order to treat disorders of cardiac rhythm. An implantable pacemaker paces the heart with timed pacing pulses. The pacing pulses can be timed relative to other pacing pulses or to sensed (intrinsic) electrical activity. If functioning properly, the pacemaker enforces a minimum heart rate to make up for the heart's inability to pace itself at an appropriate rhythm for metabolic demand. Some pacing devices synchronize pacing pulses delivered to different areas of the heart in order to coordinate the contractions. Coordinated contractions allow the heart to pump efficiently to provide sufficient cardiac output. Clinical data has shown that cardiac resynchronization, achieved through synchronized biventricular pacing, results in a significant improvement in cardiac function. Cardiac resynchronization therapy improves cardiac function in heart failure patients. Heart failure patients have reduced autonomic balance, which is associated with LV (left-ventricular) dysfunction and increased mortality.
Commonly treated conditions relate to the heart beating too fast or too slow. When the heart beats too slow, often leading to a condition referred to as bradycardia, pacing can be used to increase the intrinsic heart rate and correct the condition. When the heart beats too fast, often due to a condition referred to as tachycardia, intrinsic electrical stimulus of the heart itself, in the presence of certain myocardial substrate modifications (e.g., infarcted or non-conducting areas), can find a circuit that allows them to re-enter into the original activation circuit and re-trigger a new activation. These re-entrant circuits can lead to very fast heart rates that can be undesirable and even fatal. To correct for this condition, antitachycardia pacing (ATP) at rates higher than the tachyarrhythmia rates can be used to regain control of the heart rhythm by using specialized sequences of pulses and trains of pulses. Once the system delivering the antitachycardia fast pacing takes control of the heart, it can gradually reduce its pacing rate in the hopes that the normal sinus rhythm will take control again, and reduce the intrinsic heart rate. Antitachycardia pacing is generally used in combination with an implantable defibrillator, because the pacing burst could accelerate the arrhythmia into ventricular fibrillation.
When pacing for bradycardia, percutaneously placed pacing electrodes can be positioned in the right-side chambers (right atrium or right ventricle) of the heart. Access to such chambers is readily available through the superior vena cava, the right atrium, the tricuspid valve and then into the right ventricle. Pacing of both the right atrium and right ventricle was developed. Such dual chamber pacing resulted in better hemodynamic output than right ventricle-only pacing. In addition to treating bradycardia, dual chamber pacing maintained synchrony between the atrial and ventricular chambers.
Electrode placement in the left ventricle is normally avoided, where access is not as direct as in right ventricle placement. Moreover, emboli risk in the left ventricle is greater than in the right ventricle. Emboli that might develop in the left ventricle by reason of the electrode placement have direct access to the brain via the ascending aorta from the left ventricle. This could result in stroke.